Fig. 7
From: Vidarabine, an anti-herpes agent, prevents occlusal-disharmony-induced cardiac dysfunction in mice
This scheme illustrates the proposed role of β-AR/Gsα/AC5 signaling in the heart of BO mice. β-AR/Gsα/AC5 signaling is activated by the BO treatment, leading to oxidative stress via activation of NOX4/ASK1/p38 and phosphorylation of CaMKII (Thr-286), which mediates PLN phosphorylation at Thr-17. In addition, cAMP derived from AC5 mediates oxidative stress and PLN phosphorylation at Ser-16. These changes might cause fibrosis, myocyte apoptosis and oxidative stress in the heart of BO mice, leading to cardiac dysfunction